Beesource Beekeeping Forums banner

Coevolution of Honey Bees and Varroa Mites: A New Paper

74K views 225 replies 24 participants last post by  souficoufi 
#1 ·
Here's a beautiful new paper. Look at this statement:

"Coevolution by natural selection in this system has been hindered for European honey bee hosts since apicultural practices remove the mite and consequently the selective pressures required for such a process."

More sound backing for the understanding: treatments ('apicultural practices') prevent the rise of resistance which otherwise occurs rapidly.

Mike

Host adaptations reduce the reproductive success of Varroa
destructor in two distinct European honey bee populations
Barbara Locke, Yves Le Conte, Didier Crauser & Ingemar Fries

Ecology and Evolution 2012; 2(6):
1144–1150
http://onlinelibrary.wiley.com/doi/10.1002/ece3.248/pdf

Abstract
Honey bee societies (Apis mellifera), the ectoparasitic mite Varroa destructor, and honey bee viruses that are vectored by the mite, form a complex system of host–parasite interactions. Coevolution by natural selection in this system has been hindered for European honey bee hosts since apicultural practices remove the mite and consequently the selective pressures required for such a process. An increasing mite population means increasing transmission opportunities for viruses that can quickly develop into severe infections, killing a bee colony. Remarkably, a few subpopulations in Europe have survived mite infestation for extended periods of
over 10 years without management by beekeepers and offer the possibility to study their natural host–parasite coevolution. Our study shows that two of these "natural" honey bee populations, in Avignon, France and Gotland, Sweden, have in fact evolved resistant traits that reduce the fitness of the mite (measured as the reproductive success), thereby reducing the parasitic load within the colony to evade the development of overt viral infections. Mite reproductive success was reduced by about 30% in both populations. Detailed examinations of mite reproductive parameters suggest these geographically and genetically distinct populations favor different mechanisms of resistance, even though they have experienced similar selection pressures of mite infestation. Compared to unrelated control colonies in the same location, mites in the Avignon population had high levels of infertility while in Gotland there was a higher proportions of mites that delayed initiation of egg-laying. Possible explanations for the observed rapid coevolution are discussed.
 
See less See more
#185 ·
DWV without mites. You sampled the colony to establish that?

Two frames of brood? What was in the additional drawn frame? Just comb? a frame full of honey? Or Honey and pollen?

When you write that you took samples from the new hive, I assume you mean you took samples of bees? And what will you be doing to test them for resistance to DWV? I guess you will be looking for some sort of genetic marker or something?
 
#186 ·
We've already extracted, PCRed and run gels. We've got good extractions, amplifications, and gels.

It'll be some time before I can report any findings. It's someone else's project.

If they do a great job of it, then it can take them places.

As a side note, I have another Honeybee virus related project going on as well.

This one is more theoretical though.
 
#188 ·
sqkcrk:

There was some pollen and honey in each of the splits with an extra partially/fully drawn frame.

I took the original hive apart w/ a large carving knife, scraper, etc., I found the queen and left her with about 4 frames in the original location. Checked everything in 'good light'.

The original hive is still leaking DWV.

I've got bees from before the split, and then after the successful split from the parent and daughter colonies.

Boy, am I glad I converted a Dustbuster to a bee vac sampler.

We can do virus (RNA), target integration site (rDNA), virus vs integrated virus expression (RNA).

Personally, I only care about the target rDNA site. The other stuff has already been done by others.

My thing is catching 'instant evolution' in the act:

DWV jumping into Honeybees, because of a split, and perhaps even testing positive for DWV resistance.

Hunter et al. already found DWV in Honeybees, but I doubt that they used this kind of experimental design.

sqkcrk:

Regardless, somebody is going to learn something. :)

WLC.
 
#189 ·
Regardless someone always learns something. Quite often what someone learns is not what someone else was trying to teach. Haven't you noticed that to be true? Porejemplo, we have learned something about each other, haven't we? But, some of us have not learned what we wanted to. What can we do?
 
#190 · (Edited)
Now, for a gratuitous link for the thread:

http://www.slu.se/en/faculties/nl/a...department-of-ecology/hemsidor/locke-barbara/

I learned that we've got alot to learn about the coevolution of the Honeybee, the Varro mite, and other pathogens.

I hope to learn how to make transgenic, DWV resistant, treatment-free bees (OK, so I fed them peppermint candy) by splitting a DWV infected hive.

I think that would be alot to learn on a thread like this.
 
#191 ·
Here is something you can learn, if you will, peppermint candy has no appreciable effect on Varroa or Tracheal mites. Nor does it do any good on DWV. Lesson taught. Now it is up to the student to learn.

Check w/ Geulph University, Guelph, Ontario. I don't know if Gard Otis is still there or not, but he did a study way back in the late 1980s, putting bars of menthol into beehives to treat T. mites. No positive effects.
 
#194 ·
WLC
I have read the entirety of this thread with great interest. I have recently had some coursework in both immunology and infectious agents/virology and will attempt to reconstruct your argument for splitting infected hives to try to induce spontaneous resistance to a viral pathogen.

Your premise is bases on the assumption that it is the viruses carried and spread by the Varroa mite that are causing the damage to the bee population and not so much the mite itself. By breeding "sick" colonies, you are trying to encourage the emergence of bees that have successfully "reverse engineered" the viral RNA and inserted it into their own DNA in a way that allows them to immediately have resistance to the virus. This is a genetic mechanism that is separate and distinct from the "usual" Mendelian genetics that we are all used to- which works by breeding "the best to the best". From a Mendelian perspective, breeding impaired/sick bees is the a "very bad thing" and is the basis of much of the resistance noted in this thread to the idea of breeding sick bees. I am going to try to explain how the alternate system might work for generating resistant bees.

Bees have some (limited) ability to spontaneously develop resistance by incorporation of the virus genetic material into their own DNA is a fashion that allows them to develop innate immunity to the virus. that is to say that when the virus infects the bee, the bee already has immunity in place to immediately remove or neutralize the virus. They have to have an active infection with the virus in order for this genetic incorporation to occur (hince the splitting of sick hives). My understanding of how this happens is as follows:
1) Viral genetic material in the case of the Deformed Wing Virus is made of strands of a material called Ribonucleaic Acid, or RNA.
2) Before this genetic code can be inserted into the bee genome, it must be converted to Deoxyribonucleaic Acid or DNA. This conversion is accomplished by an enzyme called a reverse transcriptase- it takes the viral RNA strand and molecule by molecule converts it to an equivalent DNA strand.
3) In order to get the freshly minted DNA material from the virus inserted into the bee DNA genetic code, a special enzyme called a retrotransposon is utilized. This enzyme takes newly formed piece of DNA (formed from the viral RNA), and (I believe) randomly inserts it into the bee's genetic code. Once inserted, it stays.
4) The tough part is that the new DNA may or may not insert into a part of the bee DNA that is used to control the bees immune system. The bee reportedly has 10,000 genes, and if this genetic material is (randomly) inserted into most of them, it would not function in the immune system and might even be bad (or lethal) to the offspring. Eventually, after enough tries, the correct insertion would occur and the offspring would have innate resistance to the virus!
5) I think that the queen bee would have to be infected with the virus in question. In a manner that I am not completely clear on, the retrotransposon is active in the reproductive tract of the queen and is randomly inserting the genetic material into cells that divide an become eggs. It is not clear to me if each individual egg have a randomly placed piece of genetic material or if all of them have the material inserted into the same spot. This suggests that drones would be carrying the genetic material as well.
6) In order for the new innate resistance to be manifested in a colony formed by splitting, the split would have to raise a queen from brood from the prior queen. This new queen would have to bear the virus genetic material at just the right spot in her genome so that she had viral resistance. Then her offspring would have resistance-Voila- new immediate resistance to the viral pathogen!

And that is how I think it works!

Hope it helps.
TooFarGone
 
#196 · (Edited)
Mike:

"Therefore, more detailed investigations
are necessary to identify and tease apart the possible
mechanistic differences."

I was discussing one possible mechanism by which bees can evolve resistance to varroa mites: molecular immunity to the viruses that they carry via transgenesis.

My main contention is that molecular immunity to viruses by Honeybees is also better understood as a mechanism of co-evolution and resistance than any of the other mechanisms being considered.

They can't seem to be able to identify the specific genes (sequences) involved for the other mechanisms.

I've noticed that in the literature.

I gave specific evidence for co-evolution.

I've provided a mechanism for virus resistance.

It doesn't require human intervention to occur naturally in treatment-free bees.

However, I'd like to see if we can detect an actual act of 'instant evolution'.

I do understand the issues involved.

Are we clear now?

WLC.
 
#198 ·
"Therefore, more detailed investigations
are necessary to identify and tease apart the possible
mechanistic differences."

I was discussing one possible mechanism by which bees can evolve resistance to varroa mites: molecular immunity to the viruses that they carry via transgenesis.
Ok, thanks for the heads up. I'd advise: spend some time learning how to relate your thinking to the general public. We've had to pick apart for ourselves what it is your talking about. (BTW: I think this would be better expressed: 'gain resistance intially, which then enters the evolutionary mechanisms that operate through natural selection' or something of that kind.)

My main contention is that molecular immunity to viruses by Honeybees is also better understood as a mechanism of co-evolution and resistance than any of the other mechanisms being considered.
Fine. But the subject of the paper, and our interest in it, is centred alomost entirely on the mechanisms and relations that pertain to bee-mite coevolution, through the mechanism of natural selection. That subject supplies us with insights that we can take to our own treatment-free beekeeping. There is, in other words, a clear point to this thread, and a clear subject - and intention of starting the thread was to provide a forum for exploring that. As I've said, I'm interested in your input.

I'm now asking another direct question: wouldn't you agree that starting a new thread is simple and appropriate, given that several of the main posters to this thread have indicated impatience, the moderator has recommended ignoring you, and the originator has asked for you to stop interrupting the discussion?

We'd like, please, to work through the paper at our own pace, looking at the parts we can relate to our own knowledge and practices. You are constantly hijacking the space we use to do that. Again, please, start your own thread. Its easy and effective - it will give you the space you would like to talk about the things you want to talk about.

Mike
 
#199 ·
Mike:

People are asking questions because they're interested, thus the drawing out of the explanations.

Try not to be so patronizing.

My challenge to you is this:

prove to me that co-evolution is responsible for the survival of the Gotland and Avignon hives.

WLC.
 
#202 · (Edited by Moderator)
Thanks for the explanation of reverse transcriptase and retrotransposon, after 10 pages of reading on this thread I finally learned something.
[...]
...way to think outside of the box.
What I seemed to learn was that there is a 1 in 10,000 chance of a piece of the viral code making its way to an appropriate place - yielding, at this stage a 1 in 10,000 chance of what is wanted occurring. Except...

...We can't just assume that any old bit if viral code will have the desired effect. (In fact quite how a bit of viral code has the effect of supplying a resistance to the bee is not explained either.) So we also have to assign a probablity to the transposed viral code being a useful piece (and never mind the mechanics of just it works). Whatever that probability is now has to be multiplied by 10,000 (the probability of insertion happening at the right place).

That, I would guess, would bring us into the same sorts of realms as good old mutation by background radiation - one in lots and lots and lots cubed lots of times.

This rather makes a mockery of WLC's analysis of his 1 in 10 hives experiment. His is a very far from impartial 'analysis' of a very badly conducted 'experiment' on a very inadequate sample. It is, lets recall, a 'theory' supplied by several posters over the course of a week or so - WLC being unable to explain it himself.

To take another easy pot: if bees were able to gain resistance every 10 matings in 'challenged' circumstances, it follows that viral problems would be fixed before they had even arisen!

I'm all for thinking outside the box, but this box has more holes than swiss cheese.

Mike
 
#204 · (Edited by Moderator)
We've taken it and utilized it for our own purposes - to make specialised proteins that we can use.

That's not the same thing at all as incorporating it as a way of gaining resistance to the doner virus.

We gain resistance to viruses through the workings of our own immune system, by exposure mostly. But resistence is also passed down through colostrum - the first part of mother's milk. This is necessary because viruses constantly mutate - you need an up to date 'patch' as it were.

Any virus incorporated into our own code in the manner WLC suggests would be out of date within a generation or two.

Its worth reading this piece at wiki - particularly the part relating to animal husbandry. http://en.wikipedia.org/wiki/Colostrum

Mike
 
#205 ·
I wouldn't say we took it. But it got in there.

In bacteria, viruses insert themselves into the code (remember a virus is not a living thing, essentially only a section of RNA) and then may live on as part of the bacteria and its offspring indefinitely. At some point in the future, even many generations later, it can reemerge.

My breeding program takes advantage of the natural winnowing, natural exposure, and traditional breeding up of resulting performing stock.

Funny thing, back when the treatment-free thing was in its infancy, you'd hear things like 'you can't breed wolf resistant sheep.' But you can. Nobody does, but you can. You may get sheep with long legs that run fast, or that are well camouflaged, or that eat wolves, or who knows what. Once you have them though, you're going to have to work on breeding back in the traits for wool and meat production. All things considered, bees have ended up being much easier than that.
 
#207 ·
Funny thing, back when the treatment-free thing was in its infancy, you'd hear things like 'you can't breed wolf resistant sheep.'
"Now it is known that bees can be bred for resistant
behavior, so it is hard to imagine that it was at most a guess
and a hope only 17 years ago when Kefuss began to
experiment with the idea. His respected doctoral mentor,
Ruttner, opined that bees could not be bred against mites,
saying, “Sheep can’t be bred against wolves.”

[...]

From 1999 to 2005, Ralph
Buchler tested 13 lines of bees from different areas in Europe on the island of Unije in Croatia for resistance to
Varroa without treatment. Kefuss’ bees from Toulouse were the last to die out. “Ruttner told me that it turns out
that sheep can be bred against wolves.”

http://survivorstockqueens.org/John Kefuss Keeping Bees That Keep Themselves.pdf

Sheep were pretty wolf resistant from the start. Their main defence was probably their exquisite climbing ability. There's a wonderful example of the extraordinary climbing of - in this case - goats, here:

http://www.dailymail.co.uk/news/art...t-near-vertical-Cingino-dam-Italian-Alps.html

Mike
 
#206 ·
Introns help make diversity but viral code added to animal cells is different than plant and with meta-genetics and the importance of mythelation in both expression and deactivation of areas of introns because they are unfit... well its a great area of science but thinking you can split a viral infected hive and in your lifetime create a new gene from viral code is a joke the idea it will be a helpful gene is sad. dna has many repair mechanisms. the best we can hope for in our lifetime is micro-evolution as in changing the ratio or combination of genes for a better (or synergistic) effect to combat viruses and parasites.

http://www.sciencedaily.com/releases/2011/12/111204144654.htm
http://www.sciencedaily.com/releases/2009/06/090615171519.htm
mythelation
http://www.sciencedaily.com/releases/2012/03/120302101712.htm
granted in plants it may be different
http://www.sciencedaily.com/releases/2011/11/111129112329.htm

This is a great field but what you learned in school is rather useless in five years and from several of the above statements I'd say careful listening to one person or book... though I dont remember even in school being told viral dna(?) could create a intron that would make a new gene for a protein that would benifit the host... wow
 
#209 ·
In reference to the article that is the basis for this thread, my reading suggests that the Varroa mites had suppressed reproduction in the Gotland colonies and these same mites were tested in other control colonies and their reproductive success was notably improved to a statistically significant degree. This answers a criticism I have seen in other venues (and possibly this thread, I don't remember) that the "obvious" explanation for the reduced reproductive success was essentially entirely on the basis of the selection of a less fecund mite population.
 
#211 · (Edited by Moderator)
That might have been me - but it wasn't meant as a 'criticism'.

It does seem obvious to me that where bees are targetting large mite families and leaving smaller ones alone, the result will be the emergence of mite strains that have smaller families. The 'coevolution' is the result of bees effectively breeding less fecund mites.

If, as you say, the mites were tested in other colonies and found to tend to return to larger families, that would tend to confirm the hypothessis that the first (VHS) bees were responsible. (An extract would be handy)

The mechanism responsible would be the VHS bees' tendency to uncap and destroy larger mite families, but to leave small families alone. There appears to be evidence (see below) that the bees even leave alone and recap small mite families - at least I think that is what is being inferred - the writing isn't explicit.

That's how I make sense of it.

In this case I think its safe to say (against WLC's view) that co-evolution is what is being observed. We should note that this 'evolution' can switch back rapidly - there's nothing fixed about it.

BTW: We need to acknowledge the multi-layered nature of the term 'mechanism'. 'Mechanisms' are known to be tricky things to talk about. I've speculated about a 'mechanism' above, and it seems like a plausible explanation to me for how VSH 'works'. But it doesn't say anything about the lower level 'mechanism' responsible for the bees' behaviour in the first place. This is known to be genetic - because it is heritable - but the exact gene locations responsible are undiscovered as yet. So WLC, who is interested in the molecular level - is quite right in saying 'the mechanism' is unknown - at that level. It is also right to to say that part of the second-level mechanism - of how bees detect varroa in closed cells in the first place - is unclear. (The best guess as far as I know is by odour.)

Saying 'the mechanism is unknown' is true therefore in some respects, but not in others. And we must be careful not to elide - to infer unknowns from one area are unknowns in others - where things are better, even if imperfectly, understood.

Its worth bearing in mind too, none of this need concern beekeepers at all. As long as you follow the method of propagating from best - boosted if necessary by more intense breeding measures - all will be well. You don't need to know any more than how to apply to bees the dictum 'put best to best'.

Mike

http://en.wikipedia.org/wiki/Varroa_sensitive_hygiene

Bees with the trait were initially bred by the USDA Honey Bee Breeding, Genetics and Physiology Laboratory in Baton Rouge, LA from colonies in which mite populations grew only slowly.[1]

The factor causing slow mite population growth was found to be heritable[2]. The rate of mite population growth was found to be correlated with the reproductive rates of mites[1], resulting in naming the factor “suppressed mite reproduction” (SMR)[3]. It was subsequently discovered that the factor is founded on hygienic activity of adult bees[4][5], so SMR was renamed VSH.[6]

VSH activity results in (1) an abnormally low proportion of mites that produce offspring within the population that remains in capped brood and (2) reduction of the brood infestation rate by greater than 70%. The specifics of how hygienic bees detect mite infested brood currently are unknown.

Extension.org: Selecting for Varroa Sensitive Reproduction
http://www.extension.org/pages/30984/selecting-for-varroa-sensitive-hygiene
Select on mite infertility
The most reliable method is to select for a high infertility rate in the mite population (Fig. 2). We are not certain how it happens, but somehow VSH increases mite infertility. Generally, 15-25% of mites in non-resistant colonies do not lay eggs. Infertility increases to 80-100% in colonies with pure VSH queens. Mite populations eventually decline in these colonies because so few mites lay eggs.

Extension.org
http://www.extension.org/pages/30361/varroa-sensitive-hygiene-and-mite-reproduction
Removal of mite-infested brood is probably triggered by unusual odors that penetrate the cell cap to the outside where hygienic bees patrol the comb surface. We have observed that VSH bees respond vigorously to highly infested brood (e.g. 15–25 mites per 100 capped cells) that is transferred into the colony (Fig. 4). They uncap and remove many mite-infested pupae quickly. They respond with much less intensity to brood with low infestation rates (1–5 mites per 100 capped cells), probably because the chemical signals that trigger removal are less concentrated and harder to detect.

[...]
Another characteristic of VSH bees is a reduced fertility of mites, when compared to non-VSH bees. In a colony, mite fertility is reduced several weeks after introduction of VSH queens into non-selected colonies.

The VSH bees shown in Fig. 7 have about 30% reproductive mites (a normal family capable of producing a mature daughter). About 55% are infertile or non-laying mites (blue slice), and there are mites that die without producing offspring (red slice). There are also mites that produce a family, but their daughters do not mature before the bee emerges (yellow slice). These are fertile because they laid some eggs, but they are also considered non-reproductive because they will not produce even 1 mature daughter.

Sometimes, uncapped cells are recapped. VSH bees will exhibit this recapping more then non-hygienic bees, as seen in the following data (Villa et al 2010)

•Recapped cells (%)
•VSH: 38 ± 0.3 a
•Hybrid: 19 ± 0.8 ab
•Control: 17 ± 0.3 b

It is possible that uncapping and recapping interferes with mite reproduction.
 
#210 ·
That's not it.

The original 'Bond' studies claimed that the bees had adapted rather than the mites. However, they still can't provide specific evidence for the mechanism.

My own view is that they haven't demonstrated 'co-evolution' between mites and bees.

However, Maori et al. (2007) provided specific examples of co-evolution between IAPV and Honeybees. They found IAPV fragments in the Honeybee genome (providing resistance), and Honeybee sequences in IAPV!

That's co-evolution.
 
#212 ·
However, Maori et al. (2007) provided specific examples of co-evolution between IAPV and Honeybees. They found IAPV fragments in the Honeybee genome (providing resistance), and Honeybee sequences in IAPV!

That's co-evolution.
How was it demonstrated that it was the fragments found in the honeybee genome taht was providing resistance to IAPV?

Was it like your 'I made ten splits and one didn't show symptoms, so that one has become resistant.'?

Could you provide extracts of the descriptions of their tests?

Mike
 
#213 · (Edited by Moderator)
The name is WLC.

Not Bill.

It wasn't 10 splits, it was 8. We won't know if anything 'jumped' for a while.

Maori, Tanne, and Sela used Southern, Northern, and Western blot analysis, DNA sequencing, and Primer walking, to prove both co-evolution and virus resistance. You really should at least read the abstract. If you want to read the paper, you'll need institutional access. No, I won't send it to you for free.

In addition, both they and U.S. scientistis demonstrated that the IAPV fragment could be fed to bees as dsRNA to make them resistant to IAPV via RNAi.

Their work is rock solid.

The only place I can really see cooevolution in the Locke paper is the title.
[Edit]
 
#214 · (Edited)
It wasn't 10 splits, it was 8. We won't know if anything 'jumped' for a while.
Ah. How will you tell? How will you tell if the jumping has induced resistance to the virus?

Maori, Tanne, and Sela used Southern, Northern, and Western blot analysis, DNA sequencing, and Primer walking, to prove both co-evolution and virus resistance.
So you say. What I'm asking you for is _how_ they proved it with empirical tests. How many colonies did they use, how many controls did they use, how did they guard against false positives, was the testing double-blind. You know, the important bit.

You really should at least read the abstract. If you want to read the paper, you'll need institutional access. No, I won't send it to you for free.
I wasn't asking you to. I was asking you to show us (and if you can't do that with extracts, outline for us), how they 'proved' that the jumping they had induced had conferred resistance to the bees.

In addition, both they and U.S. scientistis demonstrated that the IAPV fragment could be fed to bees as dsRNA to make them resistant to IAPV via RNAi.
Again, how did they demonstrate this?

Their work is rock solid.
I have only your evaluation of that. That - given the weaknesses in your presentations and argumentation of the topic thus far - is insufficient.

The only place I can really see cooevolution in the Locke paper is the title.
Engage WLC. Take the bit I just wrote about VHS and engage with it. I've said I think that amounts to coevolution, and I've said _why_ I think that.

Its soooo easy to express an opinion; its much harder to substantiate it. But you have to to be convincing. Unless you're winning the argument with better positions than mine you're - or just by showing how mine is flawed - you're losing it. Swim or sink.

Show us _why_ you think my position - and the authors' - is wrong.

Mike
 
#215 ·
Mike:

If you want to know how Maori and the Beeologics team did it, I can only recommend that you get hold of the papers yourself.

While we might be able to do the 'jumping gene' detection and preliminary RNA based evidence for resistance, we can't do the key proof.

We can't feed jumping genes back to bees.

Anyway, I'd settle for the detection alone. It's more than enough to find something at that site in the Honeybee. No one else is looking.

Hygienic behavior was described as a possible mechanism in the Avignon hive, but not in the Gotland hive.

So, hygienic behavior is a 'possible' but not a 'definite' at Avignon.

That still leaves us with a need for a 'deeper understanding' of what is occurring at Avignon and Gotland.

I still don't see any proof for coevolution.

Just the usual conclusion: it needs more study.

WLC.
 
#216 · (Edited)
Mike:

If you want to know how Maori and the Beeologics team did it, I can only recommend that you get hold of the papers yourself.

While we might be able to do the 'jumping gene' detection and preliminary RNA based evidence for resistance, we can't do the key proof.

We can't feed jumping genes back to bees.
How would that constitute a 'key proof'? The 'key proof' would be to show that it works in real life - with real bees, under controlled conditions. Without showing that this is no more than fluff. Seriously.

WLC you're not responding to proper criticisms of your positions, nor addressing direct questions that have been put to you. (I could list them, and they probably come to 20 or 30 by now) You've barely acknowledged any of the points made by others.

This is very telling. It is natural for us to understand that trying to meet these challenges would reveal yet more weaknesses. It speaks of deep bluffing. Its also very un-academic and unscientific. You are not engaged in a discussion with us, aiming to elucidate the facts of your case. You're avoiding difficulties and simply re-stating your beliefs.

That alone wouldn't matter - although its tiresome - and greatly irritating to those whose conversations you're obstructing. But it gets worse.

You are recommending to beekeepers, under cover of scientifically dominstrated fact, an untested GM method of raising resistant bees. The method flies in the face of tested breeding husbandry - anyone following it could expect rapid stock collapse.

It may be a legitimate and valid system - if you're into GM - but -even if if works, and that appears to be unknown, its utterly unsuited to practical bee raising.

Do you understand many people have a great attachment to their stock? Many are dependent on their stock for part of their livelihood, some for their entire livelihood?

Anyway, I'd settle for the detection alone. It's more than enough to find something at that site in the Honeybee. No one else is looking.[/queen]

More than enough for what? To be able to reinforce your message to beekeepers - 'breed from 'challenged' bees and your problems will be over?

Hygienic behavior was described as a possible mechanism in the Avignon hive, but not in the Gotland hive.

So, hygienic behavior is a 'possible' but not a 'definite' at Avignon.

That still leaves us with a need for a 'deeper understanding' of what is occurring at Avignon and Gotland.

I still don't see any proof for coevolution. Just the usual conclusion: it needs more study.
'Evolution' is something that occurs from changes at many levels, in all timescales. It occurs, in a minor way in every generation. This is generally not recoginised - many people think of evolution as the cause of different species, and little else. But its much more than that: it includes the shaping, the sculpting of local populations by natural selection, as they adapt to their ever-changing environment, in each single generation.

The bees and mites at Avignon and Gotland have clearly changed in response to the pressure put upon the bees by the mites. The bee-mite pairing has 'bred' bees capable of living together. The result is a bee-mite pairing that can survive and thrive. Each has changed in response to the other. And that is called 'co-evolution.'

As to the need for further study: WLC there is pretty much always a 'need for a deeper understanding'. And it is normal practice in any academic/scientific paper to supply directions for further research in the conclusion. It doesn't indicate a confession of failure of any sort in the study being presented.

Do you not know this? In what field are your 'advanced degrees'?

Mike
 
#218 ·
I tend to answer questions selectively. You know, I avoid questions like, "Do you still kick your dog?"

Biology and Administration.

It's OK for me to test hypotheses.

I'm saying that bees are naturally transgenic. They can become resistant instantly and naturally.
I've presented it as 'evidence' for why treatment-free beekeeping can work.
I've also made the case for why Maori's work is still the strongest evidence to date for coevolution between bees and pathogens.

Now, if someone could do something similar for bees, varroa, and other pests/patohgens vis-a-vis treatment-free beekeeping, then we'd have a complete coevolution package.

The 'Bond' bees of Avignon and Gotland are well documented study hives. However, the evidence for coevolution is always presented as 'conditional' statements in the studies done.

They think that it's coevolution, but they're still studying it.

Barbara Locke has her work cut out for her.

Hygienic bees, in my opinion, are artificially selected stock bred by different programs/operations.

So, even though I bought VSH bees and didn't use standard treatment practices, I have no delusions that my bees represent a 'natural population' of bees.

They're livestock.

So, I hope that you understand my own 'informed' assessment of the state of coevolution research in bees.

The Bond bees and hygienic bees aren't the best existing evidence for it.

Maori et al. still have the best evidence of coevolution between Honeybees and a pathogen to date.

And...

You do know that they've found a bunch of transposable elements in the genomic survey of Varroa destructor? Right?

I hope that you can see that I'm advocating for a line of inquiry.

WLC.
 
#219 · (Edited)
It's OK for me to test hypotheses.
I don't know what this means?

I tend to answer questions selectively. You know, I avoid questions like, "Do you still kick your dog?"
Its fine to avoid questions of that sort. But to answer selectively on the basis 'responding to that point would undermine my case', or 'I mustn't give away that I don't know', or anything of that sort ... would amount to ... well I'm not sure I can describe it in a way that won't get this post deleted by the moderator.

Since you have a ba (minimum) in Biology you must know what I mean?

I'm saying that bees are naturally transgenic. They can become resistant instantly and naturally.
OK. But, as I've pointed out to you the odds appear to be very long indeed. Is there anything you can offer to convince me that isn't the case?

Unless the probabilities can be shortened from (my) current estimates dramatically [understatement alert], the effect of following your recommendations will be to negate (actually reverse) the well tested methods of finding health through selection for strongest - since you advocate propagating out of weakness (vulnerability to the target virus).

This, as I've pointed out to you, will have the effect of rapidly undermining apiary health. Do you wish to challenge that statement? Or does that fall the wrong side of your response-selection process for some reason?

I've presented it as 'evidence' for why treatment-free beekeeping can work.
I'm glad you put the that 'evidence' in quotes! Its nothing of the kind! It's a pet theory, the germ of a hypothesis, that has yet to be tested!

Furthermore there is already a fulsome account of why treatment-free beekeeping works. I'm not saying its complete, but the understanding of raising beneficial and required alleles in a population a la natural selection via artificial selection supplies what is widely accepted to be an adequate explanation.

This understanding is supported a large and growing body of evidence, and has ample scientific underpinning.

I've also made the case for why Maori's work is still the strongest evidence to date for coevolution between bees and pathogens.
In this, and your statement below, I think I've seen what is happening.

You reserve the term 'evolution' for such changes that are reflected in additions to the genome.

Lock, myself and others allow that the term 'evolution' can be used to describe the processes by which shifts in population genetics occur.

We allow that the raising of alleles within a population supplying resistance to varroa due to natural selection are examples of an evoltionary process. Similarly changes in (mite) fecundity might be explained by nothing more than the concentration in the mite population of alleles coding for low fertility. We describe that as evolution - referring primarily to the _process_ .

You deny that. You want to see a stronger degree of permanance to any changes before you'll allow the description 'evolution'.

Have I got that right? We're arguing at cross purposes, due to differences in what we regard as proper use of the key term?

Now, if someone could do something similar for bees, varroa, and other pests/patohgens vis-a-vis treatment-free beekeeping, then we'd have a complete coevolution package.
Do you mean make GM modifications to bee/mite/virus genomes, then their dissemination cia central breeding programs?

or

Do you mean home-made GM?

or

Or do you mean natural/semi natural (beekeeper aided) transgenesis? In which case we must return to:

a) the long odds question,

and (not 'or', _and_)

b) the difficulties inherent in selecting for health while selecting from diseased stock!

The 'Bond' bees of Avignon and Gotland are well documented study hives. However, the evidence for coevolution is always presented as 'conditional' statements in the studies done.

They think that it's coevolution, but they're still studying it. Barbara Locke has her work cut out for her.
See above the definition of 'evolution' issue.

Hygienic bees, in my opinion, are artificially selected stock bred by different programs/operations.
What about when they are ferals, exhibiting hygeinic traits as a result of natural selection?

So, even though I bought VSH bees and didn't use standard treatment practices, I have no delusions that my bees represent a 'natural population' of bees.
Nor should you. If you'd found some long-lived ferals you might take a different view. But... allowing (either of) them to interbreed with loacally raised treated stock will mean your splits will be more vulnerable to varroa, and hence to viuses. And this would be true as well for any GM bees you or anyone else makes makes.

They're livestock.
These words are keyterms, but aspects of their precise meaning is not fixed. The criteria might shift, depending on what you are interested in. There are times when in order to have clear detailed discussion you need to 'precise' your terms. 'Evolution' is here one. Thus far we've been speaking at cross purposes because we've taken fundamentally different stands on what the term does and doesn't include. Similary 'Livestock' will apply sometimes, not others.

So, I hope that you understand my own 'informed' assessment of the state of coevolution research in bees.
I might be getting there.

I hope you're beginning to understand the nature of the constraints of evidence and the difficulties in application of your ideas.

I hope that you can see that I'm advocating for a line of inquiry.
Fine. Make it. Come back and tell us about it - preferably on your own thread.

Mike
 
#220 ·
It means that I know how to formulate and test hypotheses.

Responding to some of what folks write simply goes too far afield from the main thrust of my argument or the thread.

MA. PD.

I've previously tested these bees for insertions at the site of interest and have detected many, and sequenced a few. They're already there. I've used and studied transposable elements before, and have even developed methodologies to get them to insert into sites preferentially.

Why use bees with an overt DWV infection to look for DWV insertions and even resistance? Viruses can overwhelm the bees molecularl immunity (RNAi) to such an extent, that transposable elements are no longer suppressed (my interpretation of the Johnson, 2009, paper). They start jumping. Transposable elements are known to 'jump' when sperm and eggs are being formed.

So, if you want to select for DWV resistant bees, you need to have plenty of DWV, and then you need to make new queens. You can find that evidence by taking Maori's and Hunter's approach (general structural gene insertions, or you can can use my approach (site specific). For beekeepers, it's just another Artificial selection method, but it has a solid theoretical foundation.

You don't need to be treatment-free for the above methodology to work. Sorry.

The coevolution hypothesis in the Locke paper is supported by conjectural evidence. But, they're still looking. I've endeavored to show you what evidence actually looks like.

I was describing finding jumping genes in bees, varroa and viruses that prove both recombination and resistance (coevolution).

The problem with proving coevolution in hygienice bees is that they still can't identify the genes involved. In fact, they can't even get candidate genes for hygienic traits from different studies to match. They don't have any solid evidence, yet.

Mike, since you clearly don't understand what you're reading in a scientific paper, I'll keep my own counsel on what I should be doing. :)

WLC.
 
#221 ·
It means that I know how to formulate and test hypotheses.
Then you'll know that testing a hypothesis concerning resistance in bees will involve real bees, double-blinding arrangements, control groups. So what are particulars of these test? Or, is there, in this case, some reason why such tests are not necessary.

Its a simple question.

Responding to some of what folks write simply goes too far afield from the main thrust of my argument or the thread.
That's easy. Do my questions above come into that category?

I've previously tested these bees for insertions at the site of interest and have detected many, and sequenced a few. They're already there. I've used and studied transposable elements before, and have even developed methodologies to get them to insert into sites preferentially.
And this is proof of what? Surely its wisely known that these things can be done. What's needed is confirmation that they work, and designs to show how they might be put to use.

WLC, this is all pretty typical. You've answered questions I haven't asked, and haven't responded to those I asked. You haven't addressed my criticisms, nor responded to my suggestion that there was a bit of confusion abroad due to different views of the meaning of the key term. All you've done is parroted your positions.

You've claimed 'proof' without acknowleging the point that proof lies in empirical demonstration - or explaining why that isn't necessary in this case.

This isn't dialogue. It isn't constructive. Its simply repetition of belief and refusal to take any notice of valid criticism.

Mike
 
#222 ·
Alot of very real bees died from those splits made from the DWV hive. The dark discoloration of their bodies was both obvious and disturbing.

We've got plenty of bee samples taken before during and after. However, experimental design is one of my strengths. Not yours. :)

Mike, you're confusion isn't equivalent to valid criticism.

This is simply yet another debate on treatment-free bees, and evolution, that you've lost.

I can't think of a single specific example proving the 'evolution' of resistance in treatment-free bees. There were plenty of hypotheticals though.

Pardon me if I dare to try my hand at a proof.
 
This is an older thread, you may not receive a response, and could be reviving an old thread. Please consider creating a new thread.
Top